Dehydrogenase Lab Report
The oxidative decarboxylation of Pyruvate is carried out by the pyruvate dehydrogenase complex. This multi-protein complex is composed of three enzymes; 1) pyruvate dehydrogenase, 2) dihdrolipoyl transacetylase, and 3) dihyrolipoyl dehydrogenase. The intermediate products formed by this complex are not released and remain bound to the enzyme. The breakdown of fatty acids by the β-oxidation pathway is carried out by four separate enzymes found in the mitochondrial matrix; 1) fatty acyl-CoA dehydrogenase, 2) enoyl hydratase, 3) β-hydroxyacyl-CoA dehydrogenase 4) β-ketoacyl-CoA thiolase. Each cycle of the pathway shortens the fatty acyl-CoA chain by two carbon units. This process continues until completed, resulting in the fatty acid being completely …show more content…
Human mitochondrial diseases affect people of all ages and can infect any organ in the body. To date, there is no cure for mitochondrial diseases, however there are treatments available to reduce the symptoms and the suffering of those infected. Mitochondrial disease arise when mutations occur in either mt DNA or nuclear genes that encode the mitochondrial proteins essential for the generation of ATP. Furthermore, recent research shows, that dysfunctional mitochondria in one tissue can have an effect on the whole organism (Nunnari & Suomalainen, …show more content…
As a result of the generation of mitochondrial (ROS) we see oxidative changes to proteins such as β-amyloid protein (Aβ) which may result in protein misfolding or lead to further interaction with mitochondria causing greater mitochondria dysfunction.
Parkinsons’s Disease is another neurodegenerative disease. It is an incurable, progressive brain disorder which affects the nervous system causing a slowness in movement and an involuntary shaking. It is identified by the accumulation of nerve fibers in the brain and fibrous protein deposits in the neuronal cytoplasm. Recent studies have shown (Guo et al, 2013), that mutations in mitochondrial genes are implicated in Parkinsons. A reduction of activity of Complex I of the electron transport chain and mutations in mtDNA-encoded complex I subunits and mtDNA polymerase γ are associated with Parkinson’s.
Huntington’s Disease is an inherited disorder which causes death of brain cells. Studies show that it is caused by the reduction of activity of complex II in the electron transport
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Traumatic Brain Injury Lab Report
517 Words | 3 PagesATP content and mitochondrial respiration will be measured ex vivo in rats selected from Experiment 2A at each time point (0-3 hours, 2 and 7 days) to determine the effects of melatonin on mitochondrial energetics and ROS production. Data generated will allow a comparison to be done of ex vivo ATP content and mitochondrial respiration rates in lesion versus non-lesion with in vivo measures of ATP status obtained using MRI in the same rat. Comparison will be made between saline and melatonin treated rats. Experiment 1C: To determine the impact of mono therapy (Melatonin) following TBI on apoptotic markers. Fluro Jade B and Nissl staining will be measured ex vivo in rats selected from Experiment 1A at each time point (0-3 hours, 2 and 7 days) to determine the effects of melatonin on apoptosis.
Duchenne Muscular Dystrophy
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Mitochondrial Activity Lab Report
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Encephalitis In Awakenings
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Parkinson's Disease Essay
639 Words | 3 PagesParkinson’s disease is a “disorder of the nervous system that affects movement” (Staff, 2015), but does not have an acute onset. Usually symptoms start with a slight tremor in the hands and then slowly progresses to other parts of the body (Staff, 2015). Even though most people have fast, shaking, movements, Parkinson’s can also cause stiffness or slow movements. According to Mayo Clinic Staff, early signs of Parkinson’s disease may include diminished facial expressions, absence of swaying arms when walking, and “speech may become soft or slurred” (2015). Unfortunately, Parkinson’s does not have a cure, but there are medications out there to help symptoms as well as brain surgeries.
Parkinson's Disease Research Paper
791 Words | 4 PagesIn contrast to the etiology, the epidemiology of PD is well characterized: approximately 1% of Americans over age 65 will develop Parkinson's. The disease shows no predilection for any particular ethnic group, and both genders are affected equally. Although PD can strike younger people, they represent roughly 10% of the estimated 3 million cases of PD in the United
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Neuropsychological Disorders Cause Brain Trauma
440 Words | 2 PagesBrown, Gotham & Marsden (1987) conducted a study to show how cognitive impairments can be observed in people with Parkinson’s disease. They found that the deficits of Parkinson’s disease have a close similarity to damage of the prefronatal cortex. When patients were off levodopa they had an impairment of verbal fluency. Huntingtons disease is a motor disorder that is passed down from generation with rapid deteriation that starts of as a slight fidgetiness and can cause dementia. Bossy-wetzel, Petrilli & Knott (2008) state that due to the fact that Parkinson’s disease occurs so late in life, the effect on the brain that it has is not entirely
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789 Words | 4 PagesThe onset of AD is associated with mutations four types of proteins: the precursor protein for Aβ called APP, presenilin-1 (PS1) or presenilin-2 (PS2), proteins associated with the growth of and development of nervous tissue, in apolipoprotein E, a major cholesterol carrier involved in lipid transport and injury repair in the brain, and tau protein. (13) Mutations in the proteins PS1 and PS2 enhances the processing of APP, leading to the development of large amounts of Aβ, which is toxic for the neurons. (7) Aβ can cause neurotoxic effects in many ways, including disruption of mitochondrial function by binding of the Aβ-binding alcohol dehydrogenase (ABAD) protein, induction of apoptotic genes through inhibition of Wnt, by
Cellular Respiration Research Paper
1393 Words | 6 PagesThe pyruvate molecules that were created in glycolysis are then sometimes fermented into lactic acid. Lactic acid can be used to transform lactose into lactic acid, for example in the making of yoghurt. This process is also used in animal muscles when they require extra energy in their tissue in order to run faster than oxygen can be given. C6H12O6 (glucose) > 2CH3CHOHCOOHc*lactic acid) is the net equation for glucose to lactic acid.
Essay On Parkinson's Disease
776 Words | 4 PagesParkinson’s disease is a disease in the brain that causes to kill nerve cells. These neurons are in a specific place on the brain called substantia nigari. Dopamine is a chemical produced by these neurons that allow movement. What Parkinson’s disease does to the body is lack of movement. This disease stops you from doing some things an individual does every day.
Write An Essay On Mitochondrial Disease
757 Words | 4 PagesMitochondrial disease happens when the mitochondria in a cell fail to produce enough energy for the cell to function. This results in a disease called mitochondrial disease, this is a genetic disorder with no cure. There can be many different forms of mitochondrial disease such as, Alper’s disease. Alper’s disease begins during early childhood; symptoms include increased muscle tone, seizures and loss of cognitive ability. There are many causes for the disease, with genetics, metabolic aspects and mitochondria playing an important role in the appearance of this disorder.
Parkinson's Disease Research Paper
782 Words | 4 PagesOur recent studies have shown that inflammatory cytokine TNF induces reactive oxygen species via NADPH oxidase that causes oxidation of phospholipids to phospholipid hydroperoxide and Azelaoyl phosphotidadyl choline (Scheme 1) and increases Platelet-activating Factor (PAF) in non-neuronal cells, and I expect brain and nervous tissues are also very susceptible to oxidation due to their high level of polyunsaturated fatty acids and intense consumption of oxygen. Furthermore, TNFα receptor 1 is highly expressed on dopaminergic neurons, and their expression increases in PD (). More significantly, Oxidatively truncated phospholipids are internalized, migrate to mitochondria, and then disrupt mitochondrial function, in a way aided by Bid, to initiate intrinsic apoptosis (23, 24). PAF and oxidatively truncated phospholipids, a proinflammatory lipid mediators bind to the G-protein coupled transmembrane receptor, the
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